Alcoholic hepatitis Flashcards
What is alcoholic hepatitis?
Inflammatory liver condition caused by chronic alcohol consumption.
When does alcoholic hepatitis develop?
Due to sustained long term alcohol consumption and occurs in 10-35% of heavy drinkers.
What is the pathophysiology of alcoholic hepatitis?
Liver metabolises alcohol to acetaldehyde leading to production of reactive oxygen species → hepatocyte damage → this triggers an immune response + inflammatory response → inflammation and necrosis of hepatocytes.
What’s required for development of alcoholic hepatitis?
Long history of heavy drinking of 15-20 years.
What are the main clinical features of alcoholic hepatitis?
- Jaundice - due to impaired bilirubin metabolism and excretion due to liver inflammation → buildup in the blood
- Nausea and vomiting
- RUQ pain
- Hepatomegaly - swelling due to inflammation - swelling in glissons capsule around the liver → tenderness on palpation
- Loss of appetite (weight loss)
- Fever with tachycardia
What features can you see if alcoholic hepatitis is severe?
Ascites and splenomegaly due to portal hypertension.
What bedside investigations can be done for alcoholic hepatitis?
- Abdominal exam - RUQ pain, tachycardia, hepatomegaly, ascites (shifting dullness, abdomen may be distended), jaundice
- Basic observations
What bloods are done in alcoholic hepatitis?
- FBC- showing non-megaloblastic macrocytic anaemia (sign of alcoholic liver disease)
- AST>ALT (2:1) (Make a toAST with alcohol) (both increased)
- Elevated GGT (particularly in absence of raised ALP → suggests alcohol abuse)
- Increased ALP (but to lesser degree than AST and ALT)
- Increased Bilirubin (due to cholestasis - bile flow is slowed), Decreased Albumin (hepatocytes cannot produce albumin due to damage)
- Increased PT → sensitive marker of significant liver damage. Clotting factors 2,7,9,10 are made by the liver (mainly affect PT but also APTT).
What is non-megaloblastic macrocytic anemia?
Macrocytic anaemia is a condition where the RBC are larger then normal.
Non-megaloblastic anaemia implies that the cause of the large RBC is not due to the vitamin B12 or folic acid deficiency - it is commonly associated with alcoholic liver disease and chronic use.
Why might GGT be elevated when ALP is normal?
Gamma-glutamyl transferase (GGT) it is a non specific marker of liver dysfunction and alcohol induces its activity.
GGT levels correlate with the amount and duration of alcohol consumption.
ALP is normal as it only rises with cholestasis, biliary cholangitis or any cause of a bile duct obstruction.
GGT with normal ALP → INDICATES ALCOHOL ABUSE.
What scan is done in alcoholic hepatitis?
US to check for other causes of liver impairment e.g. malignancy.
What is management in alcoholic hepatitis?
- Acute → thiamine (prevent Wernicke’s encephalopathy), vitamin C, pabrinex (vitamin replacement)
- Withdrawal Management → chlordiazepoxide (if have symptoms of withdrawal)
- Steroid Therapy (Corticosteroids - prednisolone) → reduces short-term mortality for severe alcoholic hepatitis
- Immediate cessation of alcohol use.
What withdrawal management is given in alcoholic hepatitis?
Chlordiazepoxide - if they have symptoms of withdrawal.
What measurement is used to see who would benefit from steroid therapy in acute episodes in alcoholic hepatitis?
Maddrey’s discriminant function (DF) calculated using prothrombin time and bilirubin concentration - value >32 is severe.
What complication is there for alcoholic hepatitis?
Cirrhosis
Describe the prognosis for alcoholic hepatitis.
10% mortality in 1st month.
40% mortality in first year.
If alcoholic intake continues, will progress to cirrhosis in 1-3 years.
